Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cytoplasmic lncRNAs accumulate upon ANS-induced translation elongation inhibition

ABSTRACT: Cytoplasmic lncRNAs accumulate upon ANS-induced translation elongation inhibition

PROVIDER: PRJNA839353 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19266831_1.fastq.gz	Fastqsanger.gz
	SRR19266831_2.fastq.gz	Fastqsanger.gz
	SRR19266832_1.fastq.gz	Fastqsanger.gz
	SRR19266832_2.fastq.gz	Fastqsanger.gz
	SRR19266833_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Cytoplasmic lncRNAs accumulate upon CHX-induced translation elongation inhibition

Project description:Cytoplasmic lncRNAs accumulate upon CHX-induced translation elongation inhibition

| PRJNA839352 | ENA

Cytoplasmic lncRNAs accumulate upon ANS-induced translation elongation inhibition

Project description:To investigate the role of translation in the decay of cytoplasmic lncRNAs, we performed RNA-Seq in WT and upf1-delta yeast cells, treated or not with CHX.

2024-02-20 | GSE203276 | GEO

Cytoplasmic lncRNAs accumulate upon CHX-induced translation elongation inhibition

Project description:To investigate the role of translation in the decay of cytoplasmic lncRNAs, we performed RNA-Seq in WT and upf1-delta yeast cells, treated or not with CHX.

2024-02-20 | GSE203277 | GEO

Xrn1-sensitive lncRNAs accumulate upon inactivation of Dbp2 and Mtr4

Project description:Xrn1-sensitive lncRNAs accumulate upon inactivation of Dbp2 and Mtr4

| PRJNA986459 | ENA

Expression of subtelomeric lncRNAs links telomeres maintenance with RNA decay in S. cerevisiae

Project description:Long non-coding RNAs (lncRNAs) have been shown to regulate gene expression, chromatin domains and chromosome stability in eukaryotic cells. Recent observations have reported the existence of telomere associated long ncRNAs (TERRA, telomeric repeat containing RNA) in mammalian and yeast cells but their function(s) remain(s) poorly characterized. Here, we report the existence in S. cerevisiae of several sense and antisense Cryptic Unstable Transcripts (CUTs) and Xrn1-sensitive Unstable Transcripts (XUT) initiating within the subtelomeric repeated region Y’. We show that the Y’ ncRNAs, subTERRA, are distinct from TERRA and are mainly destabilized by the general cytoplasmic and nuclear 5’- and 3’- RNA decays in a sense-dependent manner. subTERRA transcription is mainly sustained by RNAPII and subTERRA accumulate preferentially during the G1/S transition and in C-terminal rap1 mutants independently of Rap1p function in silencing. The accumulation of subTERRA in RNA decay mutants coincides with telomere misregulation: shortening of telomere length, loss of telomeric clustering in mitotic cells, indicating that subTERRA might compete with factors involved in telomere elongation, tethering and/or clustering. We propose that subtelomeric RNAs expression links telomere maintenance with RNA degradation pathways. Exmination of two yeast mutants for RNA decay.

2015-04-30 | E-GEOD-67585 | biostudies-arrayexpress

Xrn1-sensitive lncRNAs are globally insensitive to the cytoplasmic helicases Ecm32, Ski2, Slh1, Dbp1 and Dhh1

Project description:To investigate the role of cytoplasmic helicases in the decay of Xrn1-sensitive lncRNAs, we performed RNA-Seq in WT, ecm32-delta, ski2-delta, slh1-delta, dbp1-delta and dhh1-delta yeast cells.

2023-07-27 | GSE235553 | GEO

Histamine H3 receptor agonist regulates the expression of inflammation-related genes in kidney and heart of ANS-treated mice

Project description:We found the impaired renal function accompanied with severe cardiac dysfunction in mice co-treated with angiotensin II, nephrectomy and salt (ANS), and identified the increased level of plasma histamine in ANS-treated mice. Interestingly, pro-inflammatory genes were increased in kidneys of ANS-treated animals, which were down-regulated by histamine H3 receptor (H3R) agonist. Purpose: To evaluate the molecular mechanisms underlying the effect of the H3R agonist on the ANS-induced renal and cardiac inflammation, we performed a comprehensive analysis of ANS-mediated gene expression changes with/without H3R agonist in kidneys and hearts using RNA sequencing (RNA-Seq). Results: To investigate differentially expressed genes (false discovery rate (FDR) p<0.05, fold change >2) among three groups, we performed pairwise comparisons of RNA-Seq data using the CLC Genomics Workbench software. In comparison with the control of kidney group, 1,283 (1,010 up- and 273 down-regulated) unique genes were significantly changed in the ANS-treated group. Meanwhile, the data set of ANS-treated kidneys with H3R agonist revealed significant changes in 234 (65 up- and 169 down-regulated) genes as compared with the control groups. In case of hearts, the ANS-treated group revealed that 85 (66 up- and 19 down-regulated) unique genes were significantly changed compared to the control groups. Furthermore, in comparison with the ANS-treated with H3R agonist group, one up-regulated gene was significantly changed in the ANS-treated group.

2019-12-26 | GSE100635 | GEO

Real-Time Quantitative PCR Analyis of Neonatal Rat Aortic Neurospheres (ANS)

Project description:Progenitor/stem cell populations of the aorta have been poorly characterized and their self-renewal factors unknown. In this report, we demonstrate that sphere forming progenitor/stem cells, here within termed aortic neurospheres (ANS), can be cultivated from the aorta that are similar to skin-derived precursors (SKPs). Extensive mRNA transcript profiling revealed that ANS abundantly expressed the Inhibin βA transcript, of which the secreted protein dominantly formed the Inhibin βA-βA complex, or Activin A, in the proliferation medium. Co-localization of Activin A, Nestin and Sox2 was observed in the adventitial and peri-adventitial regions of the aorta, indicative of a progenitor/stem cell niche in vivo. Blockade of Activin A signaling, through the neutralization of the Type II Activin receptors ActRIIA and ActRIIB, resulted in the asymmetric differentiation, and epithelial-to-mesenchymal transition of the ANS, respectively. When treated with the latter neutralizing antibody, translocation of the ActRIIB receptor to the nucleus was observed in cells on the periphery of the sphere. Examination of the ActRIIB protein sequence showed the presence of a putative nuclear localization signal of the PY family that was conserved across species. The results from this study demonstrate that Activin A is a self-renewal factor required for maintaining ANS progenitor/stem cell identity and multipotency.

2022-07-05 | GSE207380 | GEO

Effect of global translation initiation inhibition associated to glucose starvation on cytoplasmic lncRNAs levels

Project description:To analyze the effect of global translation initiation inhibition associated to glucose deprivation on cytoplasmic lncRNAs levels, we performed RNA-Seq using WT, xrn1-delta and upf1-delta cells grown in glucose-containing complete synthetic medium (CSM) and then shifted for 16 min in glycerol- and ethanol-containing medium. In parallel, control cells were maintained for the same time in glucose-containing CSM. For the WT strains, we also included a treatment of 15 min with CHX (100 μg/ml final concentration) or an equal volume of DMSO (Mock).

2024-02-20 | GSE232893 | GEO

Xrn1-sensitive lncRNAs accumulate upon inactivation of Dbp2 and Mtr4

Project description:To investigate the role of the helicases Dbp2 and Mtr4 in the decay of Xrn1-sensitive lncRNAs, we performed RNA-Seq in yeast cells lacking Dbp2 or depleted for Mtr4.

2023-07-27 | GSE235552 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data